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Aim: In our study, we aimed to investigate the value of fetal epicardial fat thickness (EFT) and modified myocardial performance index (mod-MPI) in fetal growth restriction (FGR) that develops after the 32nd week of gestation., Materials and Methods: Fifty-six pregnant women who met the inclusion and exclusion criteria were included in the study and were divided into two groups: pregnancies diagnosed with FGR after the 32nd week of gestation (FGR group) and those without (control group). Demographic and obstetric histories, ultrasonographic and clinical characteristics, fetal EFT and mod-MPI values, and neonatal outcomes of the groups were recorded, and comparisons were made between the groups. Additionally, the diagnostic performance of fetal EFT value in late FGR was investigated., Results: The FGR group had fetal EFT that was statistically significantly lower (1.11 ± 0.21 vs. 1.34 ± 0.23, p = 0.001). The FGR group had a significantly lower isovolumetric contraction time (ICT) (31.04 ± 6.88 vs. 35.14 ± 7.58, p = 0.048). The two groups' isovolumetric relaxation time (IRT), ejection time (ET), and mod-MPI values (p values 0.871, 0.55, and 0.750, respectively) were comparable. Receiver operating characteristic (ROC) analysis at a cutoff of 1.2 revealed 76.1% sensitivity and 74.2% specificity, respectively, for the diagnostic performance of the fetal EFT value in late-onset FGR. There was a positive predictive value (PPV) and negative predictive value (NPV) of 64.0% and 83.8%, respectively., Conclusion: We found that fetal EFT was significantly lower in FGR and may be useful in diagnosing FGR. However, we observed that mode-MPI did not change in FGR., (© 2024 Wiley Periodicals LLC.)

Objective: This study aimed to evaluate fetal epicardial fat thickness (EFT) together with fetal myocardial performance index (MPI) and its effects on neonatal outcomes in obese pregnant women., Materials and Methods: A total of 102 pregnant women, 51 obese and 51 of normal weight, were included in this prospective study. Fetal EFT, and MPI measurements were performed for all patients., Results: Fetal EFT and Mod-MPI showed a statistically significant difference between obese pregnant women and the control group (p=0.0001, p=0.001). The optimal fetal EFT predictive cut-off value for the 5th-minute APGAR score below 7 was 1.22 mm, with a sensitivity of 86.96% and a specificity of 54.43% (p=0.001)., Conclusion: Fetal EFT and mod-MPI were higher in obese pregnant women. It is encouraging that fetal EFT predicts low APGAR, but more important information can be obtained if postnatal follow-up of these cardiac changes caused by obesity can be performed., Competing Interests: The authors declare that they have no conflict of interest., (Thieme. All rights reserved.)

The distinct anatomic environment in which adipose tissues arise during organogenesis is a principle determinant of their adult expansion capacity. Metabolic disease results from a deficiency in hyperplastic adipose expansion within the dermal/subcutaneous depot; thus, understanding the embryonic origins of dermal adipose is imperative. Using single-cell transcriptomics throughout murine embryogenesis, we characterized cell populations, including Bcl11b + cells, that regulate the development of dermal white adipose tissue (dWAT). We discovered that BCL11b expression modulates the Wnt signaling microenvironment to enable adipogenic differentiation in the dermal compartment. Subcutaneous and visceral adipose arises from a distinct population of Nefl + cells during embryonic organogenesis, whereas Pi16 + /Dpp4 + fibroadipogenic progenitors support obesity-stimulated hypertrophic expansion in the adult. Together, these results highlight the unique regulatory pathways used by anatomically distinct adipose depots, with important implications for human metabolic disease., (© 2024 Traynor et al.; Published by Cold Spring Harbor Laboratory Press.)

Fetal hypoxemia decreases insulin and increases cortisol and norepinephrine concentrations and may restrict growth by decreasing glucose utilization and altering substrate oxidation. Specifically, we hypothesized that hypoxemia would decrease fetal glucose oxidation and increase lactate and pyruvate production. We tested this by measuring whole body glucose oxidation and lactate production, and molecular pathways in liver, muscle, adipose, and pancreas tissues of fetuses exposed to maternal hypoxemia for 9 days (HOX) compared with control fetal sheep (CON) in late gestation. Fetuses with more severe hypoxemia had lower whole body glucose oxidation rates, and HOX fetuses had increased lactate production from glucose. In muscle and adipose tissue, expression of the glucose transporter GLUT4 was decreased. In muscle, pyruvate kinase ( PKM ) and lactate dehydrogenase B ( LDHB ) expression was decreased. In adipose tissue, LDHA and lactate transporter ( MCT1 ) expression was increased. In liver, there was decreased gene expression of PKLR and MPC2 and phosphorylation of PDH, and increased LDHA gene and LDH protein abundance. LDH activity, however, was decreased only in HOX skeletal muscle. There were no differences in basal insulin signaling across tissues, nor differences in pancreatic tissue insulin content, β-cell area, or genes regulating β-cell function. Collectively, these results demonstrate coordinated metabolic responses across tissues in the hypoxemic fetus that limit glucose oxidation and increase lactate and pyruvate production. These responses may be mediated by hypoxemia-induced endocrine responses including increased norepinephrine and cortisol, which inhibit pancreatic insulin secretion resulting in lower insulin concentrations and decreased stimulation of glucose utilization. NEW & NOTEWORTHY Hypoxemia lowered fetal glucose oxidation rates, based on severity of hypoxemia, and increased lactate production. This was supported by tissue-specific metabolic responses that may result from increased norepinephrine and cortisol concentrations, which decrease pancreatic insulin secretion and insulin concentrations and decrease glucose utilization. This highlights the vulnerability of metabolic pathways in the fetus and demonstrates that constrained glucose oxidation may represent an early event in response to sustained hypoxemia and fetal growth restriction.